scholarly journals Myocardial Ischemia on Thallium Scintigraphy in Hypertrophic Cardiomyopathy

Circulation ◽  
2001 ◽  
Vol 104 (13) ◽  
Author(s):  
John H. Haley ◽  
Todd D. Miller
CHEST Journal ◽  
1987 ◽  
Vol 92 (2) ◽  
pp. 371-374 ◽  
Author(s):  
Thomas A. Kelly ◽  
Denny D. Watson ◽  
John P. DiMarco ◽  
Robert S. Gibson

2006 ◽  
Vol 290 (3) ◽  
pp. H1064-H1070 ◽  
Author(s):  
Shinsuke Kido ◽  
Naoyuki Hasebe ◽  
Yoshinao Ishii ◽  
Kenjiro Kikuchi

The aim of this study was to investigate what factor determines tachycardia-induced secretion of atrial and brain natriuretic peptides (ANP and BNP, respectively) in patients with hypertrophic cardiomyopathy (HCM). HCM patients with normal left ventricular (LV) systolic function and intact coronary artery ( n = 22) underwent rapid atrial pacing test. The cardiac secretion of ANP and BNP and the lactate extraction ratio (LER) were evaluated by using blood samples from the coronary sinus and aorta. LV end-diastolic pressure (LVEDP) and the time constant of LV relaxation of tau were measured by a catheter-tip transducer. These parameters were compared with normal controls ( n = 8). HCM patients were divided into obstructive (HOCM) and nonobstructive (HNCM) groups. The cardiac secretion of ANP was significantly increased by rapid pacing in HOCM from 384 ± 101 to 1,268 ± 334 pg/ml ( P < 0.05); however, it was not significant in control and HNCM groups. In contrast, the cardiac secretion of BNP was fairly constant and rather significantly decreased in HCM ( P < 0.01). The cardiac ANP secretion was significantly correlated with changes in LER ( r = −0.57, P < 0.01) and tau ( r = 0.73, P < 0.001) in HCM patients. Tachycardia potentiates the cardiac secretion of ANP, not BNP, in patients with HCM, particularly when it induces myocardial ischemia and LV diastolic dysfunction.


2009 ◽  
Vol 2 (4) ◽  
pp. 452-461 ◽  
Author(s):  
Franco Cecchi ◽  
Aurelio Sgalambro ◽  
Massimo Baldi ◽  
Barbara Sotgia ◽  
Davide Antoniucci ◽  
...  

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S Aguiar Rosa ◽  
L Branco ◽  
A Galrinho ◽  
A Fiarresga ◽  
L Lopes ◽  
...  

Abstract Background Myocardial ischemia constitutes one of the most important pathophysiological features in hypertrophic cardiomyopathy (HCM). Chronic and recurrent myocardial ischemia leads to fibrosis, which may culminate in myocardial dysfunction. Objective To analyse the relationship between left ventricular (LV) morphology and systolic performance and coronary microcirculatory dysfunction in HCM. Methods The present study prospectively included HCM patients (P) who underwent transthoracic echocardiography. Left ventricular (LV) function was evaluated by ejection fraction (LVEF), global longitudinal strain (GLS) and tissue Doppler septal and lateral s’. The evaluation of coronary flow velocity reserve (CFVR) was performed in apical three chambers view for the left anterior descending (LAD) artery and in an apical three chambers view for the posterior descending (PD) artery. Diastolic coronary flow velocity was measured in basal conditions and in hyperemia, induced by adenosine perfusion (0.14 mg/kg/min intravenously, during 2 minutes). Absolute CFVR was calculated as the ratio of hyperemic to basal peak diastolic flow velocities; relative CFVR was calculated as the ratio between CFVR LAD and CFVR PD. Results 23 P were enrolled (57% male, mean age 57.9 ± 13.7 years). Asymmetric septal hypertrophy was verified in 70% of P, with maximal wall thickness of 21.6 ± 4.3mm. Obstructive HCM was documented in 35% of patients. CFV was successfully measured in the LAD in all patients, but only in 70% of patients in the PD due to technical issues related to poor acoustic window and anatomical constraints. 78% of P (n = 18) presented CFVR &lt;2, denoting microcirculatory dysfunction. Relative CFVR (LAD CFVR/ PD CFVR) was ≥1 in 43% of P. P with maximal wall thickness (MWT)&gt;20mm presented higher CFV PD at baseline (46.5 ± 17.4 vs 32.5 ± 12.6 cm/s; p = 0.072), lower CFVR PD (1.3 ± 0.3 vs 2.5 ± 0.8; p = 0.003) and greater regional difference of microcirculation (relative CFVR 1.4 ± 0.6 vs 0.8 ± 0.3; p = 0.048). At baseline conditions, CFV LAD was higher in obstructive HCM (44.0 ± 4.8 vs 35.3 ± 10.6 cm/s; p = 0.040). P with impairment in global longitudinal strain (GLS&gt;-18%) had higher basal CFV LAD (40.1 ± 8.6 vs 30.0 ± 12.2 cm/s; p = 0.059) and PD (44.5 ± 15.2 vs 20.0 ± 5.0 cm/s; p = 0.015) but lower CFVR PD (1.5 ± 0.5 vs 2.8 ± 1.1; p = 0.039). The reduction in CFVR PD was also noted in P with time to peak longitudinal strain dispersion &gt;90mseg (CFVR PD 1.2 ± 0.2vs1.9 ± 0.9;p = 0.012). Conclusion Higher CFV at baseline was noted in P with greater MWT, obstructive HCM and worse GLS. Coronary microcirculatory dysfunction was associated with the degree of LV hypertrophy and impairment in LV systolic performance.


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